Periodontitis and lipopolysaccharides: How far have we understood?

S. Banavar, E. Tan, F. Davamani, S. Khoo
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Abstract

Periodontitis is a ubiquitous chronic inflammatory worldwide disease. The multiplicity of gram-negative microbiomes and their endotoxins, such as lipopolysaccharides (LPS), play a crucial role in its pathogenesis. The detection and consequent effects of LPS occur either via membrane-based cluster of differentiation 14 (CD14)/myeloid differentiation factor 2 (MD2)/Toll-like receptor (TLR)-4 complex activation or through intracellular cytosolic LPS detection that further cascades its effects, resulting in a variety of cell death processes, including apoptosis, pyroptosis, necroptosis, NETosis, and their crosstalk. Irrespective of the detection of LPS, the cellular response is for protecting and resolving the inflammation. However, chronic and exaggerated responses in periodontitis result in the destruction of periodontal structures. This review summarizes the extracellular and cytosolic detection of LPS and its further consequences. Then, it sheds light on methods reported to mitigate the adverse effects of LPS.
牙周炎与脂多糖:我们了解了多少?
牙周炎是一种普遍存在的全球性慢性炎症性疾病。革兰氏阴性微生物群及其内毒素(如脂多糖(LPS))的多样性在牙周炎的发病机制中起着至关重要的作用。LPS 的检测和随之产生的效应可通过膜上的分化簇 14(CD14)/髓系分化因子 2(MD2)/类托尔受体(TLR)-4 复合物激活,也可通过细胞内的细胞膜 LPS 检测,从而进一步产生级联效应,导致多种细胞死亡过程,包括细胞凋亡、嗜热细胞增多症、坏死细胞增多症、网状细胞增多症以及它们之间的相互影响。无论检测到何种 LPS,细胞反应都是为了保护和消除炎症。然而,牙周炎中的慢性和夸张反应会导致牙周结构的破坏。本综述总结了 LPS 的细胞外和细胞膜检测及其进一步的后果。然后,它揭示了所报道的减轻 LPS 负面影响的方法。
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